In animal models of experimental diabetic nephropathy, AngII induced activation of NADPH oxidase and eNOS uncoupling serves as the major source of superoxide, and the blockade of AngII signaling ameliorates eNOS uncoupling by increased tetrahydrobiopterin levels with following restoration of NO bioavailability and improved glomerular hemodynamics [39]–[40]. Here, FMO5 is linked to diabetic kidney disease.